Resolvin D1 mitigates energy metabolism disorder after ischemia–reperfusion of the rat lung

Journal of Translational Medicine

Research

Maoping Chu¹  Xingti Hu²  Jie Xia²  Qingwang Hua²  Qifeng Zhao²  Jie Du²  Zhiyong Lin²  Guowei Wu²  Weixi Zhang³  Leping Ye³  Ji Wu⁴ 

[1] The Department of Children’s Cardiovascular Medicine, Children’s Heart Center, the Second Affiliated Hospital, Yuying Children’s Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People’s Republic of China;The Department of Children’s Cardiovascular and Thoracic Surgery, Children’s Heart Center, the Second Affiliated Hospital, Yuying Children’s Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People’s Republic of China;The Department of Children’s Respiration Medicine, The Second Affiliated Hospital and Yuying Children’s Hospital, Wenzhou Medical University, 325000, Wenzhou, People’s Republic of China;Wuhan Medical & Healthcare Center for Woman and Children, 430015, Wuhan, People’s Republic of China;

关键词: Resolvin;    Lung ischemia/reperfusion injury;    Inflammatory factor;    Oxidative stress;    Energy metabolism;   

DOI  :  10.1186/s12967-016-0835-7

 received in 2015-12-02, accepted in 2016-03-16,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundEnergy metabolism disorder is a critical process in lung ischemia–reperfusion injury (LIRI). This study was aimed to determine the effects of resolvin D1 (RvD1) on the energy metabolism in LIRI.MethodsForty Sprague–Dawley rats were divided into the following groups: Sham group; untreated ischemia–reperfusion (IR) control; IR treated with normal saline (IR-NS); and IR treated with RvD1 (IR-RV) (100 μg/kg, iv). LIRI and energy metabolism disorder were determined in these rats.ResultsThe results revealed that the levels of interleukin (IL)-1β, tumor necrosis factor-α, IL-10, monocyte chemoattractant protein-1, macrophage inflammatory protein-2, cytokine-induced neutrophil chemoattractant-1, injured alveoli rate, apoptosis index, pulmonary permeability index, malondialdehyde, ADP, and lactic acid were increased, whereas the levels of ATP, ATP/ADP, glycogen, Na+–K+-ATPase, superoxide dismutase, glutathione peroxidase activity, pulmonary surfactant associated protein-A, and oxygenation index were decreased in rats with LIRI. Except for IL-10, all these biomarkers of LIRI and its related energy metabolism disorder were significantly inhibited by RvD1 treatment. In addition, histological analysis via hematoxylin–eosin staining, and transmission electron microscopy confirmed that IR-induced structure damages of lung tissues were reduced by RvD1.ConclusionRvD1 improves the energy metabolism of LIRI disturbance, protects the mitochondrial structure and function, increases the ATP, glycogen content and Na+–K+-ATPase activity of lung tissue, balances the ratio of ATP/ADP and finally decreases the rate of apoptosis, resulting in the protection of IR-induced lung injury. The improved energy metabolism after LIRI may be related to the reduced inflammatory response, the balance of the oxidative/antioxidant and the pro-inflammatory/anti-inflammatory systems in rats.

【 授权许可】

CC BY   
© Zhao et al. 2016